Premium
Induced Pulp Lesion Promotes Alteration of the Insulin Signal and Causes Insulin Resistance
Author(s) -
Sumida Doris Hissako,
Astolphi Rafael Dias,
Curbete Mariane Machado,
Chiba Fernando Yamamoto,
Melo Yamamoto Aline Pedro,
Prieto Annelise Katrine Carrara,
Cintra Luciano Tavares Angelo
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1109.6
Subject(s) - insulin resistance , lesion , insulin , medicine , endocrinology , pulp (tooth) , insulin tolerance test , adipose tissue , insulin receptor , inflammation , stimulation , insulin sensitivity , dentistry , surgery
The current study aimed to investigate if a pulp lesion, which is a local inflammatory disease, can promote alterations in insulin signal and insulin sensitivity (IS). Twenty‐eight two‐month‐old (230g) Wistar male rats were randomly divided into a control group (CN) and a pulp lesion group (PL). PL group was submitted to pulp lesion induction through the opening of the coronal pulp chamber of the upper right first molars by using a dental handpiece, followed by its exposure to oral cavity, promoting bacterial contamination and chronic inflammation. Thirty days after PL induction, the following evaluations were performed: 1) pp185 (IRS‐1/IRS‐2) tyrosine phosphorylation status (pp185 P‐Tyr), after insulin stimulation, in periepididimal white adipose tissue (WAT) and gastrocnemius muscle (G) by Western Blotting analysis; 2) IS determination by intravenous insulin tolerance test. The results showed that PL promoted: 1) a significant decrease (p<0.05) in the pp185 P‐Tyr in WAT (CN=152.9±12.7 vs PL=111.3±10.2 arbitrary units/ìg of protein, n=7) and in G (CN=133.1±9.1 vs PL=103.7±7.6 arbitrary units/ìg of protein, n=7); 2) a significant difference (p<0.05) in the IS (glucose disappearance speed rate: CN=3.04±0.26 vs PL=1.97±0.25 %min, n=7). These data suggest that PL is capable of changing insulin signal in both WAT and G, and causing insulin resistance in rats. Financial Support: FAPESP (2011/04255–8).